Clinical tools do not predict pathological complete response in patients with esophageal squamous cell cancer treated with definitive chemoradiotherapy.

Chemoradiotherapy for locally advanced esophageal squamous cell carcinoma is associated with high rates of pathological complete response. A pathological complete response is recognized to be an important predictor of improved survival, to the extent that observation rather than surgery is advocated by some in patients with presumed pathological complete response based on their clinical response. The goal of this study was to look at the ability of clinical variables to predict pathological complete response after chemoradiotherapy for locally advanced esophageal squamous cell carcinoma. We reviewed retrospectively patients with locally advanced esophageal squamous cell carcinoma who underwent chemoradiotherapy followed by surgery and compared those with pathological complete response to patients with residual disease. Between January 1996 and December 2010, 116 patients met inclusion criteria. Fifty-six percent of patients had a pathological complete response and a median survival of 128.1 months versus 28.4 months in patients with residual disease. When compared with patients with residual disease, patients with a pathological complete response had a lower post-neoadjuvant positron emission tomography (PET) maximum standardized uptake value (SUVmax), a larger decrease in PET SUVmax, a less thick tumor on post-chemoradiotherapy computed tomography and a higher rate of normal appearing post-chemoradiotherapy endoscopy with benign biopsy of the tumor bed. However, none of these characteristics alone was able to correctly identify patients with a pathological complete response, and none has significant specificity. Although the rate of pathological complete response after chemoradiotherapy is high in patients with esophageal squamous cell carcinoma, the ability of identifying patients with pathological complete response is limited. A reduction of the PET SUVmax by >70%, a normal appearing endoscopic examination, and no residual disease on biopsy all were seen in >65% of the patients with a pathological complete response. Even if these findings were unable to confirm the absence of residual disease in the primary tumor, they can help guide expectant management in high-risk patients.

Prospective multivariate analysis of clinical, endoscopic, and histological factors predictive of the development of Barrett's multifocal high-grade dysplasia or adenocarcinoma.

OBJECTIVE: Our goal was a prospective follow-up of Barrett's esophagus to determine what clinical, endoscopic, and histological features at the time of initial diagnosis are predictive of the development of Barrett's adenocarcinoma or multifocal high-grade dysplasia (HGD). METHODS: Newly diagnosed Barrett's esophagus patients were prospectively followed with a standardized endoscopic and bioptic surveillance protocol. Features examined by chi2 and stepwise logistic regression analyses as potential predictors the development of multifocal HGD or adenocarcinoma included age, length of Barrett's segment, hiatal hernia size, severity of dysplasia at diagnosis, severity of dysplasia during surveillance, and type of long-term medical treatment. RESULTS: One hundred-eight Barrett's patients have had follow-up ranging from 12 months to 101 months (mean +/- SD, 39.9+/-20.8 months), for a total of 361.8 patient-years. Overall, five patients developed multifocal HGD and five developed adenocarcinoma. The incidence of adenocarcinoma as well as multifocal HGD was 1 per 71.9 patient-years. Chi2 analysis showed progression to Barrett's multifocal HGD/adenocarcinoma was associated with hiatal hernia (p = 0.02), the length of Barrett's (p = 0.001), the presence of dysplasia at diagnoses (p < 0.001) or anytime during surveillance (p < 0.001). Stepwise logistic regression analysis revealed progression to multifocal HGD or adenocarcinoma was significantly and independently associated with presence of dysplasia at diagnosis (p < 0.0001) or anytime during follow-up (p < 0.03), hiatal hernia size (p < 0.02, for hernia > or =3 cm), and length of Barrett's (p = 0.009, >2 cm). CONCLUSIONS: Endoscopic and histological features of Barrett's esophagus patients at initial diagnosis are predictive of risk of progression to cancer.

Prospective multivariate analysis of factors predictive of complete regression of Barrett's esophagus.

OBJECTIVE: Demographic, endoscopic, and histological features of Barrett's esophagus at initial diagnosis were examined for their ability to predict complete endoscopic and histological regression of Barrett's during long-term follow-up. METHODS: Barrett's patients who have been followed up for a minimum of 2 yr and who have had at least two follow-up surveillance examinations were included in the analysis. Complete regression of Barrett's was defined as total disappearance of all tongues and patches of Barrett's epithelium at endoscopy (confirmed with Lugol's iodine) in conjunction with only squamous epithelium on biopsy. Chi2 and stepwise logistic regression analyses were performed on the following clinical, endoscopic, and histological variables with regards to their ability to predict complete Barrett's regression: patient age in years (<65 or > or =65), length in cm of Barrett's (< or =2, >2<6, and > or =6), presence of a hiatal hernia (yes or no), presence of dysplasia at diagnosis (yes or no), and type of long-term medical treatment (histamine antagonists, proton pump inhibitor [PPI], or PPI and cisapride). RESULTS: Ninety-nine patients, all men with a mean age +/- SD in years of 61.6+/-13.1 have been followed prospectively for 24-106 months (mean +/- SD, 48.0+/-19.8). Seven patients have had complete regression of Barrett's. Univariate analysis showed that complete regression of Barrett's was associated only with absence of a hiatal hernia (p = 0.012). Stepwise logistic regression analysis revealed that complete regression was significantly and independently associated again only with absence of a hiatal hernia (p = 0.025). Stepwise logistic regression analysis utilizing only hiatal hernia (yes vs no) and length of Barrett's (<6 cm vs > or =6 cm) as variables revealed that absence of a hiatal hernia (p = 0.0447) and shorter lengths (<6 cm) of Barrett's (p = 0.0418) were significantly and independently predictive of complete Barrett's regression. CONCLUSIONS: The absence of a hiatal hernia was noted to be the most important factor associated with Barrett's regression. Complete regression of Barrett's esophagus occurs in a minority of patients, primarily in those with no hiatal hernia and shorter lengths of Barrett's epithelium.

Dermatomyositis in association with tubulovillous adenoma: resolution after resection of adenoma.

Dermatomyositis (DM) has been associated with gastrointestinal malignancy but not with polyps or adenoma. We report a case of villous adenoma associated with DM. An 80-year-old white woman was referred for a rash of 2 months' duration that was suggestive of DM. On examination, Gottron's papules and heliotrope rash were seen. Muscle strength was 4/5 in the proximal upper and lower extremities. Despite normal muscle enzyme values, electromyographic and nerve conduction studies were supportive of the diagnosis of DM. DM was confirmed by deltoid muscle biopsy. Heme-positive stool was seen on rectal examination. Colonoscopy revealed a large tubulovillous adenoma in the cecum, which was resected. The patient was given oral prednisone, 60 mg/day. Within 4 weeks after surgery, steroids were tapered to one third the original dose. Within 9 months, steroid therapy had been discontinued with no evidence of disease activity.

Incidence and management of esophageal stricture formation, ulcer bleeding, perforation, and massive hematoma formation from sclerotherapy versus band ligation.

OBJECTIVES: The aim of this study was to compare the incidence and endoscopic management of esophageal stricture formation, significant ulcer bleeding, massive esophageal hematoma, and perforation resulting from endoscopic band ligation or sclerotherapy of esophageal varices. METHODS: Consecutive esophagogastroduodenoscopies in which band ligation or sclerotherapy was performed for acute or obliterative therapy were entered into a computerized endoscopy database during a 7-yr period. Patients were excluded if they died within 72 h of treatment session from complications unrelated to the procedure. Sclerotherapy was performed using a 25-gauge needle with 1.5% sodium tetradecyl sulfate and banding was primarily performed with a Wilson-Cook 6 or 10 shooter. Complications were assessed at scheduled endoscopy and outpatient clinic visits, review of quality assurance data tallied on a monthly basis, and patient records. RESULTS: Two hundred twenty-one cases of sclerotherapy were performed in 59 patients compared to 110 cases of band ligation in 52 patients. Five patients were excluded because of death within 72 h of the procedure. The incidence of complications from sclerotherapy:banding on a per patient basis included: esophageal stricture formation 25.6%:1.9%, ulcer bleed 25.4%:5.7%, esophageal perforation 2.2%:0%, and massive esophageal hematoma 1.6%:0%. A significant difference in complications between sclerotherapy and band ligation was noted for both stricture formation (p < 0.0005) and ulcer bleeding (p < 0.0001). The majority of ulcer bleeds required no therapeutic intervention, whereas stricture formation required multiple dilation sessions. CONCLUSIONS: Band ligation has a significantly lower incidence of stricture formation and ulcer bleeding compared to sclerotherapy. The majority of complications can be managed with endoscopic interventions.

Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma.

OBJECTIVE: This study was undertaken to prospectively determine the prevalence of gastric H. pylori infection in Barrett's esophagus and Barrett's complicated by dysplasia or adenocarcinoma. METHODS: The prevalence of H. pylori was determined in Barrett's esophagus patients compared to a control population of patients with gastroesophageal reflux disease (GERD) only. All patients had a minimum of 10 gastric surveillance biopsies obtained. H. pylori colonization was determined upon the basis of hematoxylin and eosin and use of a modified Giemsa and or Steiner's silver stain of all gastric biopsy specimens. RESULTS: Two hundred and eighty-nine Barrett's patients and 217 GERD control patients were included in the study. H. pylori was found in 95/289 (32.9%) of the Barrett's patients, compared with 96/217 (44.2%) of the GERD controls (NS). Forty-seven of the Barrett's patients had low-grade dysplasia/indefinite dysplasia, 14 high-grade dysplasia, and 20 Barrett's adenocarcinoma. When Barrett's was subgrouped according to absence of dysplasia, and presence of low-grade dysplasia, high-grade dysplasia, or adenocarcinoma, H. pylori prevalence was found to be significantly less for patients with Barrett's high-grade dysplasia (14.3%) and adenocarcinoma (15.0%) versus patients with GERD alone (44.2%), Barrett's alone (35.1%), or Barrett's with low-grade dysplasia (36.2%) (p = 0.016). This difference could not be explained by differences between Barrett's esophagus patients infected with H. pylori and those who were not with respect to gender, smoking history, alcohol consumption, use of proton pump inhibitor, or length of Barrett's mucosa. CONCLUSIONS: Barrett's high-grade dysplasia and adenocarcinoma are significantly more prevalent in patients who are not infected with H. pylori. H. pylori appears to have a protective effect against the development of Barrett's adenocarcinoma.